Tpl2 is activated by FcgammaR signals in macrophages and that its activation by these signals is required for ERK activation, cytoplasmic Ca(2+) influx, the induction of cytokine and coreceptor gene expression, and phagocytosis.

CRP antagonism of eNOS is mediated by coupling of FcgammaRI to FcgammaRIIB by Src kinase and activation of inositol 5'-phosphatase 1, and consistent with this mechanism, both FcgammaRI and FcgammaRIIB are required for CRP to blunt endothelial repair in vivo.

IgG FcgammaRI (CD64) is a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages overexpressing miR-127.

This review notes that the role of murine FcgammaRI differs considerably from human, based on sequence data, existence of the FcgammaRI variable region, and overview of disease models.

CD64 expression in macrophages is critical for the onset of meningitis by Escherichia coli K1.